Patogenesa pnykt jantung rematik,

gagal jantung, cor pulmonal,

endocarditis bakterialis
Patologi anatomi
FK UISU
2009
RHEUMATIC HEART DISEASE
Acute, immunologically mediated, multisystem
inflammatory disease group A streptococcal
pharyngitis after an interval of a few weeks
7/15/2014 2
Departemen Pathology Anatomy -
Cardiovascular
PENYAKIT JANTUNG REMATIK
REMATIK FEVER : PENY.RADANG SISTEMIK
NON SUPURATIVE BERHBNGAN DGN
INFEKSI STREPTOKOKUS HEMOLITIKUS
GROUP A & MERUPAKAN REAKSI
IMUNOLOGI DGN SERANGAN DEMAM & DI
SELINGI REMISI YG LAMA
R.F MERUPAKAN PENY.KOLLAGEN YG
MENGENAI : - PERSENDIAN - COR
- KULIT - SEROSA
- P.DRH - PARU
Only 3% group A streptococcal pharyngitis RF
Initial reactivation with subsequent pharyngeal infections

Ab >< M protein cross reaction with glycoprotein :
Heart
Joints & others

Onset : 2-3 weeks after infection Streptococci (-) in lesion
Chronic valvular
deformities
HD in acute phase
(Acute rheumatic carditis)
Rheumatic Fever may cause
7/15/2014 4
Departemen Pathology Anatomy -
Cardiovascular
7/15/2014 5
Departemen Pathology Anatomy -
Cardiovascular
7/15/2014
Departemen Pathology Anatomy -
Cardiovascular
6
INSIDEN :
* 5-15 THN 90% * KEMISKINAN
* OVERCROWDED SANITASI LINGK.
* GIZI * UMUR * SEX

PERUBAHAN RADANG REMATIK
DEGENERASI MUKOID
NECROSIS FIBRINOID
DEGENERASI HIALIN KOLLAGEN

ETIOLOGI
R.F. TIMBUL 1-4 MGG SETELAH INFEKSI
KUMAN STREPTO. ( PHARYNGITIS, TOSILITIS,
SCARLATINA) REAKSI AGAB NECROSIS
ALLERGIC FOCAL YANG DITANDAI TITER ASTO
MORPHOLOGI
KELAINAN KHAS & PATOGNOMONIS : ASCHAFF
BODY FOKUS DEGENERASI FIBRINOID YG
DIKELILINGI INFILTRAT RDG
FOKUS INI DIJUMPAI DI :
- JANTUNG - SINOVIAL SENDI
- TENDON FASCIA - JAR.IKAT LAIN T.U:
PERIVASKULAR & SUB
ENDOCARDIAL
Characteristic :
Inflammatory in 3 layers of heart (Pancarditis)

Hallmark of ARC : (Aschoff bodies)
Acute Rheumatic Carditis (ARC)
Multiple foci of inflammation within connective tissue of
heart
Central focus fibrinoid necrosis
Surrounded by :
Mononucleous
Anitschkow cells
(large histiocyte, vesicular nuclei, abundant basophilic
cytoplasm)
7/15/2014 10
Departemen Pathology Anatomy -
Cardiovascular
Pericardial involment
Fibrinous
pericarditis
Serous/Sero-
sanguineous
effusion
Manifested grossly &
microscopically :
7/15/2014 11
Departemen Pathology Anatomy -
Cardiovascular
Endocardium
Valvular inflammation tends to : mitral & aortic valves
The valve predisposes :
Small vegetations (valve closure) = verrucous endocarditis

7/15/2014 12
Departemen Pathology Anatomy -
Cardiovascular
Subcutaneous nodules / erythema marginatum
Pulmonary
Manifested by chronic inflmmation & fibrinous
inflammation of pleural surface

Skin
Arthritis of the large joints
Self limited, does not chronic deformity

7/15/2014 13
Departemen Pathology Anatomy -
Cardiovascular
7/15/2014 14
Departemen Pathology Anatomy -
Cardiovascular
PERTUMBUHAN ASCHOF BODY DLM 3 STD:

1. PHASE EXUDATIVE: FOKUS NECROSIS DI
KELILINGI SEL PMN, LIMFOSIT & PLASMA
2. PHASE PROLIFERATIVE : NECROSIS
SENTRAL DIKELILINGI SEL LIMFOSIT,
FIBROBLAST, SEL ANITSCHKOW MYOCYT ES =
CATER PILLAR CELL= SEL MESENCHYMAL
BESAR SEL DATIA ASCHOFF,
INTI BANYAK DIAGNOSTIK KHAS RHEUMATIK
FEVER

3. PHASE PENYEMBUHAN
* FIBROSIS
* HIALINISASI FOKUS NEKROSIS
* KDG LIMFOSIT (+)
MORFOLOGI JANTUNG
- CARDITIS RHEUMATICA TIMBUL PD R.F
- KETIGA LAP. JTG DPT TERKENA
- PERICARDIUM DG REAKSI RDG EXUDAT
FIBRINOSA & SEROFIBRINOSA YG TDK
MERATAPERICARDITIS BREAD DAN
BUTTER DPT: - SEMBUH SEMPURNA
- PERLEKATAN FOKAL
- BERCAK PENEBALAN
- MYOCARDIUM : * EXUDATIVE
* FIBROSIS YG PROGRESIF
- ENDOCARDIUM ASPEK YG BERBAHAYA:
* BERCAK PADA ATRIUM MC.CALLUM
* KERUSAKAN KATUB
KATUB MITRAL, AORTA
VEGETASI FIBROTIK, CALCIFIC
KATUB TRICUSPIDAL STENOSIS
CORDA TENDINEA MEMENDEK
& MENEBAL
TONJOLAN VEGETASI DPT MENGENAI
DAERAH KULIT, SUBCUTIS DG 1-4 CM :
SUBCUTANEUS NODULE

KLINIS : CRITERIA MAYOR JONES
1. POLYARTHRITIS MIGRANS 85 %
2. CARDITIS 65 %
3. CHOREA SYDENHAM
4. SUBCUTANEUS NODULER
5. ERYTHEMA MARGINATUM


KLINIS : CRITERIA MINOR JONES
1. LEUKOCYTOSIS
2. LED
3. ASTO
4. DEMAM
5. ARTHRALGIA
6. P.R. INTERVAL MEMANJANG
7. ERYTHEMA
KEMATIAN OK:
DECOMPENSASI CORDIS
EMBOLI THROMBUS KE OTAK/ GINJAL
ENDOCARDITIS BACTERIALIS
STENOSIS MITRALIS
PAYAH JANTUNG
CONGESTIVE HEART FAILURE
KETIDAK MAMPUAN OTOT JTG MEMOMPA
DRH YG CUKUP BAGI TUBUH
MEKANISME KOMPENSASI MYOCARD :
1. PENINGKATAN FREG. KONTRAKSI
2. DILATASI VENTRIKEL
3. HIPERTROFI OTOT JANTUNG
Otot hipertropi :
O2>>
Respon stimulasi
Inotropic activity
PAYAH JANTUNG
PENGOSONGAN TAK SEMPURNA
DILATASI BERLEBIHAN
Freq> menyebabkan tdk
cukup waktu
pengosongan ventrikel
waktu systole
Peninggian kontraksi
residual darah di
ventrikel >>
GAGAL BILA :
CHF MERUPAKAN MANIFESTASI :
1. ARTERIOSCLEROTIC HEART DISEASE
2. CARDIOMYOPATHY
* MYOCARDITIS
* DEGENERATIVE CARDIOMYOPATHY
- METABOLIC & NUTRITIONAL
- INFILTRATIVE PROSES
AMYLOID & GLYCOGEN
- NEUROMUSCULER DISEASE
- TOXIC INVOLVEMENTS
ALKOHOLIC

3. ENDOCARDIAL FIBROELASTOSIS
4. EXTRA CARDIAL :
- HIPERTENSI
- COR PULMONALE
ETIOLOGI D.C
D.C KANAN D.C KIRI
1.LUNG DISEASE COR 1. ISCHEMIC HEART
PULMONALE DISEASE
2. MITRAL STENOSIS 2. SYSTEMIC HYPER
TENSION
3.CONG.HEART DISEASE 3.KELAINAN KATUB
AORTA &MITRAL
4. MYOCARDITIS 4. CONG.HEART DIS
5. KELAINAN KATUB 5. ENDOCARDITIS
TRICUSPID.PULMONAL
6. AKIBAT PENY.JTG KIRI 6. SYPHILIS HEART
DISEASE
EFEK D.C KANAN
LOW OUT PUT OXYGENASI


ATRIUM KANAN
SYSTEMIK VEIN
BENDUNGAN VENA
EDEMA
PORTAL SYSTEM
* HEPATOSPLENOMEGALI
* CARDIAC CIRRHOSIS
* ASCITES
RV FAILURE
EFEK D.C. KIRI
TEKANAN ARTERI PULMONAL
DYSPNOE
KONGESTI P.DRH PARU
ATRIUM KIRI



LOW OUT PUT
ANOXIA
PARU : - KAPILER BERKELOK
- ANEURYSMA
- HEMORRHAGIC
- HEART FAILURE CELL
- FIBROSIS
OTAK : HYPOXIA
GINJAL : HYPOXIA


LV FAILURE
COR PULMONALE
HIPERTROPI VENTRIKEL KANAN OK.
KELAINAN PD PARU
ETIOLOGI
1. AKUT : EMBOLISME PARU MASIF SHG
VENTRIKEL KANAN DILATASI
2. KHRONIS : - PENY. P.DRH PARU
- PENY PARU KHRONIS
- KELAINAN THORAX

Ad.1. PENYAKIT P.DRH PARU
*THROMBOSIS ARTERI BESAR/KECIL DIFFUSE
* EMBOLISME
* VASCULITIS DIFFUSE
* FIBROSIS : - SARCOIDOSIS - ASBESITOSIS
- RADIASI - BERRYLLIOSIS
Ad.2. PENYAKIT PARU KHRONIS
* EMPHYSEMA
* BRONCHITIS CHRONIC
* FIBROSIS PRU OK. TBC
* SARCOIDOSIS
* PNEUMONIA BERAT
* RESEKSI PARU
Ad. 3. KELAINAN THORAX
* PENEBALAN PLEURA BILATERAL
* KELAINAN SARAF:
- POLIOMYELITIS
- MYASTHENIA GRAVIS
- DISTROFI OTOT
- KYPHOSCOLIOSIS
KLINIS
1. SESAK NAFAS
2. PEMBLH DRH MELEBAR
3. EDEMA
4. ASCITES
5. HYDROTHORAX
6. HEPATOSPLENOMEGALI

Infective Endocarditis
Caused by bacteria
Acute Sub-acute
High virulence
(Staph. Aureus)
Previously abnormal valve
Low virulence
(-Hemolytic Streptococcus)
Infection of the cardiac valve /mural surface of the
endocardium thrombotic (debris+organism) [term
vegetation]
7/15/2014 30
Departemen Pathology Anatomy -
Cardiovascular
Etiology
Bacteriemia
IV Drug Abuse
Dental Surgery
Catheter
Brushung teeth
Risk Preexisting cardiac abnormal
Prosthetic heart valves
I V drug abuser
7/15/2014 31
Departemen Pathology Anatomy -
Cardiovascular
Morphology
Vegetations :
Bacteria or other organism
Single / multiple
May involved : > 1 valve
Most common : Aortic & Mitra
RV valve drug abuser
Fungal
7/15/2014 32
Departemen Pathology Anatomy -
Cardiovascular
Acute Endocarditis
Classic vegetation
Begins : small excrescences
indistinguishable from NBTE (Non Bacterial Thrombotic
Endocarditis)
Infection may extend through :
Valve myocardium abscess peri-valvular (ring
abscess)

Microscopic :
Bacterial, fibrin, blood
Extends beyond avasc valve neutrophil response
Systemic emboli brain, kidney, myocard infarct
abscesses

7/15/2014 33
Departemen Pathology Anatomy -
Cardiovascular
7/15/2014 34
Departemen Pathology Anatomy -
Cardiovascular
7/15/2014 35
Departemen Pathology Anatomy -
Cardiovascular